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Pure platelet-rich plasma promotes semaphorin-3A expression: a novel insight to ameliorate intervertebral disk
Jie Huang1,2, Shi-Lin Lian1, Jia-Heng Han1,2
1Orthopedics of TCM Senior Department, The Sixth Medical Center of PLA General Hospital, Beijing, 100048, China.
Introduction:
Intervertebral disk degeneration (IVDD) can be effectively treated using platelet-rich plasma (PRP). While the exact process is fully understood, it is believed that using pure PRP (P-PRP) without leukocytes is a better option for preventing IVDD. Semaphorin-3A (Sema3A), an inhibitor of angiogenesis and innervation, is essential for preserving IVDD's homeostasis. Whether PRP prevents IVDD by modifying Sema3A has yet to receive much research. This work aims to clarify how P-PRP affects Sema3A when IVDD develops in vitro.
Methods:
Nucleus pulposus cells (NPCs) isolated from 8-week-old male Sprague-Dawley rats were exposed to 10 ng/ml IL-1β and then treated with P-PRP or leukocyte platelet-rich plasma (L-PRP) in vitro, followed by measuring cell proliferation, apoptosis and microstructures, inflammatory gene and Sema3A expression, as well as anabolic and catabolic protein expression by immunostaining, quantitative real-time polymerase chain reaction (qPCR), western blot, and enzyme-linked immunosorbent assay (ELISA).
Results:
In comparison with L-PRP, P-PRP had a higher concentration of growth factors but a lower concentration of inflammatory substances. P-PRP increased the proliferation of NPCs, while IL-1 relieved the amount of apoptosis due to its intervention. Anabolic genes, aggrecan, and collagen II had higher expression levels. MMP-3 and ADAMTS-4, two catabolic or inflammatory genes, showed lower expression levels. Sema3A activity was enhanced after P-PRP injection, whereas CD31 and NF200 expression levels were suppressed.
Conclusions:
P-PRP enhanced the performance of NPCs in IVDD by modifying the NF-κB signaling pathway and encouraging Sema3A expression, which may offer new therapy options for IVDD.
The Translational Potential Of This Article:
The findings provide a new therapeutic target for the treatment of IVDD and show a novel light on the probable mechanism of PRP and the function of Sema3A in the progression of IVDD.
